Due to the COVID-19 pandemic, planned medical and surgical activities are being postponed. For the dermatology community, this interruption to the healthcare system can lead to delays in the diagnosis and treatment of melanoma. Neglecting melanoma during this crisis can result in increased mortality, morbidity and healthcare costs. With the COVID-19 pandemic evolving and no clear solutions in sight, it is time for the prospective evaluation of teledermatology. However, dermatologists should be cautious and continue seeing patients with pigmented lesions in person due to the necessity of early surgical intervention.
ARTICLE HISTORY
PMM2-CDG patients have phosphomannomutase (Pmm2) deficiency, with developmental and N-linked glycosylation defects attributed to depletion of mannose-1-phosphate and downstream lipid-linked oligosaccharides (LLOs). This, the first PMM2-CDG zebrafish model, shows, unexpectedly, that accumulation of the Pmm2 substrate mannose-6-phosphate explains LLO deficiency.
Aquaporin- (AQP) 3, a water and glycerol channel, plays an important role in epidermal function, with studies showing its involvement in keratinocyte proliferation, differentiation, and migration and in epidermal wound healing and barrier repair. Increasing speculation about the use of histone deacetylase (HDAC) inhibitors to treat skin diseases led us to investigate HDAC's role in the regulation of AQP3. The broad-spectrum HDAC inhibitor suberoylanilide hydroxamic acid induced AQP3 mRNA and protein expression in a dose- and time-dependent manner in normal keratinocytes. The SAHA-induced increase in AQP3 levels resulted in enhanced [H]glycerol uptake in normal but not in AQP3-knockout keratinocytes, confirming that the expressed AQP3 was functional. Use of HDAC inhibitors with different specificities limited our exploration of the responsible HDAC member to HDAC1, HDAC2, or HDAC3. Cre-recombinase-mediated knockdown and overexpression of HDAC3 suggested a role for HDAC3 in suppressing AQP3 expression basally. Further investigation implicated p53 as a transcription factor involved in regulating HDAC inhibitor-induced AQP3 expression. Thus, our study supports the regulation of AQP3 expression by HDAC3 and p53. Because suberoylanilide hydroxamic acid is already approved to treat cutaneous T-cell lymphoma, it could potentially be used as a therapy for skin diseases like psoriasis, where AQP3 is abnormally expressed.
Topical corticosteroid phobia may lead to poor adherence, resulting in persistent disease and escalation to systemic agents. The aim of this paper was to review current literature to assess topical steroid phobia prevalence, populations most at risk, reasons behind steroid phobia, and interventions to reduce it. A systematic search of PubMed, Ovid (Journals@Ovid, MEDLINE), ScienceDirect, and Web of Science was performed. Studies ranged from May 2000 to February 2021. In total, 37 articles met the inclusion criteria. There was inter-study variation in the way steroid phobia is defined, from concern to irrational fear. The worldwide prevalence of topical steroid phobia ranges from 31 to 95.7% and does not differ with patient race/ethnicity or dermatological condition. Female patients and caregivers, and those who have experienced side effects of topical corticosteroids are most likely to express steroid phobia. Reasons for steroid phobia include lack of education, fear of side effects, polypharmacy, misinformation, negative experience with topical steroids, and frequently changing of clinics. Successful interventions to address steroid phobia include patient education in the form of educational videos followed by individualized oral education based on concerns, and demonstrations of application of topical steroids. Multiple interventions address topical corticosteroid phobia and improve adherence of topical corticosteroids in the management of dermatological conditions. Providers should screen patients for steroid phobia, especially in populations particularly at risk. Interventions using patient education should be individualized based on concerns expressed during screening. Further research should investigate if reducing steroid phobia can in fact improve long-term adherence.
An infection with the varicella-zoster virus (VZV) causes both varicella and herpes zoster (HZ). Although rare, the development of HZ does occur during pregnancy. Maternal HZ does not result in increased foetal mortality, and the passage of VZV to the foetus rarely occurs. However, HZ does increase maternal morbidity. Upon infection with HZ, patients typically present with a viral prodrome preceding the appearance of the characteristic zoster rash. HZ is usually diagnosed clinically by the zoster rash, but can also be confirmed by a polymerase chain reaction and an enzyme-linked immunosorbent assay. Pregnant women with an uncomplicated HZ should be treated with oral acyclovir. The major complications of HZ are subacute herpetic neuralgia and post-herpetic neuralgia. Other complications include zoster ophthalmicus, disseminated HZ and secondary bacterial infections. Regarding prophylaxis, the varicella and the zoster vaccines are not recommended for pregnant women, and it is important to advise non-immune pregnant women to avoid an exposure to VZV. Although HZ infection has a minimal effect on the foetus, maternal HZ and its complications cause a significant burden. It is important to focus care on the mother with appropriate treatment and management of complications as they develop.
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